Abstract
Alzheimer’s disease (AD) is the most prominent dementia-related disease and characterized by the presence of insoluble amyloid beta peptide (Aβ) fibers in or around the brain neurons of the affected person. Therefore, agent(s) capable of inhibiting brain amyloid deposition might delay the occurrence or retard the progress forwards of AD and related neurobehavioral symptoms. Here, we report whether, chronic oral administration of Syzygium cumini (locally known as Jam)-seed extract exerts protection against the progressive cognitive decline in the Aβ1-40-infused AD model rats. After 12 weeks of feeding with S. cumini seed extract (at 300 mg/kg BW), we evaluated the learning-related memory of the rats by 8-arm radial maze task, where we determined two types of memory errors, namely reference memory errors (RMEs) and working memory errors (WMEs). After completion of memory tests, rats were sacrificed and the levels of lipid peroxide (LPO), the Aβ1-40-burden, Aβ1-40-oligomers, proinflammatory TNFα, brain derived neurotrophic factor (BDNF), Tyrosine-kinase B (TrkB), postsynaptic-density protein 95 (PSD-95) and Synapse-associated protein (SNAP-25) were determined in the corticohippocampal tissues of the brain. In addition, in vitro antioxidative effects of S. cumini seed extract were evaluated. The oral administration of S. cumini extract significantly increased the memory-related learning ability of the AD model rats, concomitantly with reductions in the levels of corticohippocampal Aβ1-40-burden and Aβ1-40-oligomers. Furthermore, the extract suppressed the levels of TNFα and LPO in the corticohippocampal tissues of the AD rats and also the later in the plasma, suggesting an anti-oxidative and anti-inflammatory activities of the S. cumini extract in the brains of AD model rats. S. cumini extract also increased the levels of brain cognition and memory-related proteins, including BDNF, TrKB, PSD-95 and SNAP-25. We thus suggest that S. cumini-seed extract could be used in neurobehavioral deficits and associated pathogenesis of Alzheimer’s disease.
Highlights
The pathological hallmarks of Alzheimer disease (AD) brain include amyloid neuritic plaques and neurofibrillar tangles, concurrently with progressive loss of neurons and memory-related learning ability of the patients [1]
After 12 weeks of feeding with S. cumini seed extract, we evaluated the learning-related memory of the rats by 8-arm radial maze task, where we determined two types of memory errors, namely reference memory errors (RMEs) and working memory errors (WMEs)
No significant differences were observed in body weight or food intake, measured after 12 wks, between Control (Aβ1-40 + Vehicle-administered) and S. cumini seed extract-administered Alzheimer’s disease (AD) model rats (P < 0.05)
Summary
The pathological hallmarks of Alzheimer disease (AD) brain include amyloid neuritic plaques and neurofibrillar tangles, concurrently with progressive loss of neurons and memory-related learning ability of the patients [1]. The free radicals cause oxidation of lipids [10] [11], proteins [12] [13] and DNA/RNA [14] [15] of the neurons, which become very vulnerable to death in AD In this regard, it is plausible that antioxidant therapy would provide an important beneficial effect on the memory decline of AD patients. Several studies have focused that vitamin E attenuates the toxic effects of amyloid peptide and improves cognitive performance, with a concurrent suppression of lipid peroxidation [16]-[22]
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